Effect of single nucleotide polymorphism in thrombin-activatable fibrinolysis inhibitor on the risk of diabetic macrovascular disease.

Abstract

Hypofibrinolysis is commonly found in patients with diabetes mellitus and is associated with the increased risk for many diabetic complications. An important inhibitor of fibrinolysis, thrombin-activatable fibrinolysis inhibitor (TAFI), participates in hypofibrinolysis in diabetes mellitus and may be involved in diabetic macrovascular disease. The present study was designed to determine whether TAFI polymorphisms (505G/A and 1040C/T) and TAFI levels are correlated with the development of type 2 diabetes mellitus (T2DM) and macrovascular diseases (MVDs). A total of 249 clinical samples were collected, including 102 healthy individuals (H group), 44 T2DM patients without MVD (T group) and 103 T2DM patients with MVD (M group). The 505G/A polymorphism was equally represented in the three groups. In contrast, analysis of the 1040C/T polymorphism revealed a statistically lower percentage of the T allele in the M group than in the H group (P = 0.014). This difference was due to decreased T/T homozygotes in the M groups compared with the H group (P = 0.029). The antigen TAFI level was 31.72 ± 13.64% in the H group, 62.56 ± 18.77% in the T group (P < 0.05, compared with the H group) and 63.70 ± 15.76% in the M group (P < 0.05, compared with the H group). As high plasma TAFI level is associated with the increasing risk of T2DM, it may thus serve as a potential marker for the diagnosis of T2DM.